Strain Name:

B6N.129S1-Casp3tm1Flv/J

Stock Number:

006233

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Availability:

Repository- Live

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Brain development in Casp3-deficient mice shows a variety of hyperplasias and disorganized cell deployment, and ovaries from female homozygotes show aberrant development. These mutant mice may be useful in studies of apoptosis, ovarian follicle and corpus luteum development, and eye and ear development

Description

Strain Information

Former Names B6.129S1-Casp3tm1Flv/J    (Changed: 14-OCT-13 )
Type Congenic; Mutant Strain; Targeted Mutation;
Additional information on Genetically Engineered and Mutant Mice.
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Additional information on Congenic nomenclature.
Mating SystemHeterozygote x Homozygote         (Female x Male)   30-AUG-10
Mating SystemHeterozygote x Heterozygote         (Female x Male)   15-MAY-09
Specieslaboratory mouse
GenerationN10+N1F15 (21-DEC-12)
Generation Definitions
 
Donating InvestigatorDr. Richard A. Flavell,   Yale University School of Medicine

Description
On this C57BL/6 congenic background, homozygotes are viable, fertile, and reach adulthood, but females reported display suboptimal mothering instincts. Functional endogenous protein and mRNA are absent from all tissues tested. Homozygous mice are resistant to in vivo cerebral ischemia/reperfusion and in vitro oxygen-glucose deprivation. Ovaries from female homozygotes show aberrant atretic follicles associated with a granulosa cell-intrinsic defect in apoptosis as well as defective corpus luteum regression. Homozygous mice are congenitally deaf with hair cell defects in the Organ of Corti. Optic lens formation/morphology also is abnormal with cataracts at the anterior lens pole. Of note, these mice lack the embryonic/perinatal-lethal brain pathology observed in mutant mice on the 129 and mixed B6;129 genetic backgrounds. These mutant mice may be useful in studies of apoptosis, ovarian follicle and corpus luteum development, and eye and ear development.

Development
A targeting vector was designed to replace the caspase protease-conserved catalytic site of the endogenous gene with a PGK-neo cassette. The construct was electroporated into 129S1/Sv-derived W9.5 embryonic stem (ES) cells. Correctly targeted ES cells were injected into blastocysts, and the resulting chimeric males were bred to C57BL/6 females. Heterozygous mice were backcrossed to C57BL/6 mice for ten generations (see SNP results below) prior to sending females and males to The Jackson Laboratory Repository in 2006. Upon arrival, these females and males were used to establish our living mouse colony.

A 32 SNP (single nucleotide polymorphism) panel analysis, with 27 markers covering all 19 chromosomes and the X chromosome, as well as 5 markers that distinguish between the C57BL/6J and C57BL/6N substrains, was performed on the rederived living colony at The Jackson Laboratory Repository. While the 27 markers throughout the genome suggested a C57BL/6 genetic background, all 5 markers that determine C57BL/6J from C57BL/6N were found to be C57BL/6N allele-type. These data suggest the mice sent to The Jackson Laboratory Repository were on a C57BL/6N genetic background, the living colony is on a C57BL/6N genetic background, and the sperm frozen in 2008 is on a C57BL/6N genetic background.

Control Information

  Control
   005304 C57BL/6NJ
 
  Considerations for Choosing Controls

Phenotype

Phenotype Information

View Mammalian Phenotype Terms

Mammalian Phenotype Terms provided by MGI
      assigned by genotype

Casp3tm1Flv/Casp3+

        B6.129S1-Casp3tm1Flv
  • hearing/vestibular/ear phenotype
  • *normal* hearing/vestibular/ear phenotype
    • hearing and cochlear morphology normal   (MGI Ref ID J:68122)

Casp3tm1Flv/Casp3tm1Flv

        B6.129S1-Casp3tm1Flv
  • reproductive system phenotype
  • *normal* reproductive system phenotype   (MGI Ref ID J:70205)
    • normal fertility and viable for more than 6 months   (MGI Ref ID J:101037)
    • normal ovarian architecture with normal numbers of nonatretic primordial, primary, and small preantral follicles   (MGI Ref ID J:101037)
    • normal oocyte apoptosis   (MGI Ref ID J:101037)
    • abnormal ovarian follicle morphology
      • shrunken and disorganized atretic follicles lacking blood cell infiltration   (MGI Ref ID J:70205)
      • abnormal granulosa cell morphology
        • granulosa cells of atretic follicles are not eliminated by apoptosis and when cultured in the absence of serum fail to complete nuclear fragmentation after initial DNA condensation   (MGI Ref ID J:70205)
  • vision/eye phenotype
  • *normal* vision/eye phenotype
    • the size of the lens organelle free zone is normal   (MGI Ref ID J:101037)
    • abnormal lens development
      • slight reduction in lysis of fluorogenic substrate DEVD-AMC in both the core and cortex of the lens   (MGI Ref ID J:101037)
    • abnormal lens epithelium morphology
      • the epithelium at the anterior lens pole is multilayered and disorganized and the lens capsule above the opaque region has irregular folds   (MGI Ref ID J:101037)
    • cataracts
      • marked cataracts on the optic acis due to accumulation of epithelial cells at the anterior pole of the lens evident by the end of the first postnatal week, mature by 3 weeks of age, but most 6 month to 2 year old homozygotes no longer have cataracts   (MGI Ref ID J:101037)
  • hearing/vestibular/ear phenotype
  • abnormal auditory brainstem response waveform shape
    • ABR analysis at 2 weeks of age shows atypical waves at all frequencies with sound pressures above 70 dB   (MGI Ref ID J:68122)
  • abnormal ear morphology   (MGI Ref ID J:68122)
    • abnormal organ of Corti morphology
      • the greater epithelial ridge persists at 2 weeks of age throughout all turns of the cochlea   (MGI Ref ID J:68122)
      • the tunnel of Corti and other pericellular spaces are collapsed at 5 weeks of age   (MGI Ref ID J:68122)
      • hyperplasia and stratified arrangement of border cells throughout all turns of the cochlea at 2 and 5 weeks of age   (MGI Ref ID J:68122)
      • abnormal outer hair cell stereociliary bundle morphology   (MGI Ref ID J:68122)
        • fused outer hair cell stereocilia
          • at 2 weeks of age there is fusion of stereocilia and at 5 weeks of age all outer hair cell stereocilia are fused at the tips to an unidentified V shaped object   (MGI Ref ID J:68122)
      • cochlear inner hair cell degeneration
        • at 5 weeks of age degeneration of inner hair cells is apparent with only 1 row of inner hair cells present in the apical to middle turn   (MGI Ref ID J:68122)
      • cochlear outer hair cell degeneration
        • at 5 weeks of age degeneration of outer hair cells is apparent with only 3 rows of outer hair cells present in the apical to middle turn   (MGI Ref ID J:68122)
    • cochlear degeneration   (MGI Ref ID J:68122)
  • deafness   (MGI Ref ID J:68122)
  • increased or absent threshold for auditory brainstem response
    • at 5 weeks of age no significant waves are detected even at 100 dB   (MGI Ref ID J:68122)
  • nervous system phenotype
  • abnormal outer hair cell stereociliary bundle morphology   (MGI Ref ID J:68122)
    • fused outer hair cell stereocilia
      • at 2 weeks of age there is fusion of stereocilia and at 5 weeks of age all outer hair cell stereocilia are fused at the tips to an unidentified V shaped object   (MGI Ref ID J:68122)
  • cochlear ganglion degeneration
    • at 5 weeks of age neurons are lost from the basal spiral ganglion   (MGI Ref ID J:68122)
  • cochlear inner hair cell degeneration
    • at 5 weeks of age degeneration of inner hair cells is apparent with only 1 row of inner hair cells present in the apical to middle turn   (MGI Ref ID J:68122)
  • cochlear outer hair cell degeneration
    • at 5 weeks of age degeneration of outer hair cells is apparent with only 3 rows of outer hair cells present in the apical to middle turn   (MGI Ref ID J:68122)
  • endocrine/exocrine gland phenotype
  • abnormal ovarian follicle morphology
    • shrunken and disorganized atretic follicles lacking blood cell infiltration   (MGI Ref ID J:70205)
    • abnormal granulosa cell morphology
      • granulosa cells of atretic follicles are not eliminated by apoptosis and when cultured in the absence of serum fail to complete nuclear fragmentation after initial DNA condensation   (MGI Ref ID J:70205)
  • cellular phenotype
  • abnormal apoptosis
    • hemorrhagic response and destruction of the hepatic enothelium and subsequent death in response to injection with anti-Fas antibody Jo2 are delayed at least 12 hours relative to that in wildtype mice and the apoptotic pathway aberrently involves activation, but not altered expression, of caspases 2, 6, and 7   (MGI Ref ID J:65496)
    • mouse embryonic fibroblasts treated to initiate apoptosis fail to exhibit DNA fragmentation   (MGI Ref ID J:105496)
    • decreased apoptosis
      • following UV irradiation and staurosporine treatment, mouse embryonic fibroblasts (MEFs) exhibit increased survival compared to wild type MEFs but not as much as Casp7tm1Flv MEFs   (MGI Ref ID J:105496)

Casp3tm1Flv/Casp3tm1Flv

        B6N.129S1-Casp3tm1Flv/J
  • cellular phenotype
  • decreased keratinocyte apoptosis
    • mice exhibit decreased sunburn cells with reduced apoptotic keratinocytes generated by UV-B in the skin compared with wild-type mice   (MGI Ref ID J:189241)
  • increased cardiomyocyte apoptosis
    • in mice treated with doxorubicin   (MGI Ref ID J:189241)
  • increased sensitivity to induced cell death
    • in the cardiomyocytes of mice treated with doxorubicin   (MGI Ref ID J:189241)
    • increased cellular sensitivity to ultraviolet irradiation
      • mice exhibit decreased sunburn cells with reduced apoptotic keratinocytes generated by UV-B in the skin compared with wild-type mice   (MGI Ref ID J:189241)
      • mice exposed to UV-B radiation exhibit increased keratinocytes undergoing necrosis-like death compared with wild-type mice   (MGI Ref ID J:189241)
      • mice exposed to UV-B radiation exhibit increased cell death (apoptotic and necrosis-like combined) compared with wild-type mice   (MGI Ref ID J:189241)
  • cardiovascular system phenotype
  • increased cardiomyocyte apoptosis
    • in mice treated with doxorubicin   (MGI Ref ID J:189241)
  • integument phenotype
  • abnormal keratinocyte physiology
    • mice exposed to UV-B radiation exhibit increased keratinocytes undergoing necrosis-like death compared with wild-type mice   (MGI Ref ID J:189241)
    • decreased keratinocyte apoptosis
      • mice exhibit decreased sunburn cells with reduced apoptotic keratinocytes generated by UV-B in the skin compared with wild-type mice   (MGI Ref ID J:189241)
  • muscle phenotype
  • increased cardiomyocyte apoptosis
    • in mice treated with doxorubicin   (MGI Ref ID J:189241)

The following phenotype information is associated with a similar, but not exact match to this JAX® Mice strain.

Casp3tm1Flv/Casp3+

        involves: 129S1/Sv * C57BL/6J
  • craniofacial phenotype
  • abnormal sagittal suture morphology
    • incomplete closure of sagittal suture of anterior frontal bone at 7 weeks of age   (MGI Ref ID J:94703)
  • cranioschisis   (MGI Ref ID J:94703)
  • skeleton phenotype
  • abnormal bone ossification
    • reduced bone marrow density   (MGI Ref ID J:94703)
    • impaired osteogenic differentiation   (MGI Ref ID J:94703)
    • reduced trabecular thickness at 3 weeks of age   (MGI Ref ID J:94703)
  • abnormal bone remodeling   (MGI Ref ID J:94703)
  • abnormal sagittal suture morphology
    • incomplete closure of sagittal suture of anterior frontal bone at 7 weeks of age   (MGI Ref ID J:94703)
  • cranioschisis   (MGI Ref ID J:94703)
  • decreased bone mineral density
    • decreased bone mineral density with age with onset beginning at 3 weeks of age   (MGI Ref ID J:94703)

Casp3tm1Flv/Casp3tm1Flv

        involves: 129S1/Sv * C57BL/6
  • mortality/aging
  • complete postnatal lethality
    • animals surviving to birth die between 1-3 weeks of age   (MGI Ref ID J:36821)
  • partial prenatal lethality
    • incomplete penetrance with only 7% homozygous offspring from heterozygote x heterozygote breeders   (MGI Ref ID J:36821)
  • growth/size/body phenotype
  • decreased body size
    • smaller than littermates   (MGI Ref ID J:36821)
  • vision/eye phenotype
  • *normal* vision/eye phenotype
    • normal cell number and apoptotic kinetics within the retinal ganglion cell layer and normal width of the nerve fiber and plexiform layers   (MGI Ref ID J:88367)
    • abnormal eye morphology
      • protrusions of the neuroepithelium in the retina, causing compression on the lens   (MGI Ref ID J:36821)
      • abnormal eye development
        • delayed regression of vitreal vasculature   (MGI Ref ID J:88367)
        • abnormal optic stalk morphology
          • optic stalk contains fewer pyknotic cells and is much larger than in wild-type   (MGI Ref ID J:36821)
      • abnormal retina morphology
        • retinal dysplasia near the optic nerve ranging from absence of retinal pigment epithelium to whorled and folded neuroretina   (MGI Ref ID J:88367)
        • in severe cases, the posterior retina is folded and elevated at the optic nerve head   (MGI Ref ID J:88367)
        • abnormal retinal inner nuclear layer morphology
          • delayed apoptotic kinetics result in thickened inner nuclear layer at 5 days of age which resolves after 13 days of age   (MGI Ref ID J:88367)
        • abnormal retinal pigment epithelium morphology
          • absence of the retinal pigment epithelium in a region encircling the optic nerve   (MGI Ref ID J:88367)
      • microphthalmia
        • eyes are 85% to 90% smaller than those of heterozygotes or wild-type   (MGI Ref ID J:88367)
  • nervous system phenotype
  • *normal* nervous system phenotype
    • normal cell number and apoptotic kinetics within the retinal ganglion cell layer and normal width of the nerve fiber and plexiform layers   (MGI Ref ID J:88367)
    • abnormal brain morphology
      • multiple indentations and ectopic cell masses in the cerebrum mantel   (MGI Ref ID J:36821)
      • protrusion of brain tissue from the skull at the frontal bone area   (MGI Ref ID J:36821)
      • abnormal brainstem morphology
        • increase in cell number and density of the brainstem at E12   (MGI Ref ID J:36821)
      • abnormal cerebellar granule layer morphology
        • thickness of the internal granular layer is increased   (MGI Ref ID J:36821)
      • abnormal cerebellar molecular layer
        • numerous spindle-shaped granule cells are seen traversing the molecular layer   (MGI Ref ID J:36821)
      • abnormal cerebellum development
        • the germinal layer is thick and mitotically active at P16, at a time when it is normally absent, and spindle-shaped granule cells traverse the molecular layer   (MGI Ref ID J:36821)
        • abnormal cerebellum external granule cell layer morphology
          • the germinal layer is thick and mitotically active at P16, at a time when it is normally absent   (MGI Ref ID J:36821)
      • abnormal forebrain morphology
        • ectopic cell masses are found between the cerebral cortex, the hippocampus and the striatum   (MGI Ref ID J:36821)
        • abnormal diencephalon morphology
          • thicker diencephalic wall with supernumerary cell masses is seen at E12   (MGI Ref ID J:36821)
      • hydroencephaly
        • diencephalic lumen is frequently obstructed at E17   (MGI Ref ID J:36821)
  • skeleton phenotype
  • abnormal bone ossification
    • reduced trabecular thickness   (MGI Ref ID J:94703)
    • reduced bone volume to tissue volume ratio   (MGI Ref ID J:94703)
    • delayed bone ossification
      • evident at E14.5 in skull, metacarpi, phalanges, and sternum and at E17.5 in interparietal bones and metatarsi   (MGI Ref ID J:94703)
  • abnormal osteoclast physiology
    • osteoclast activity is reduced, most likely due to dysfunctional preosteoblastic cells   (MGI Ref ID J:94703)
  • abnormal sagittal suture morphology
    • open sagittal suture of anterior frontal bone at 7 weeks of age   (MGI Ref ID J:94703)
  • abnormal skeleton development
    • skeleton is smaller than normal at 1 week of age   (MGI Ref ID J:94703)
    • abnormal bone marrow development
      • increased replicative senescence in bone marrow stromal stem cells from attenuated cell cycle   (MGI Ref ID J:94703)
  • cranioschisis
    • either completely open sagittal suture or incomplete closure at 7 weeks of age   (MGI Ref ID J:94703)
  • decreased trabecular bone thickness   (MGI Ref ID J:94703)
  • craniofacial phenotype
  • abnormal sagittal suture morphology
    • open sagittal suture of anterior frontal bone at 7 weeks of age   (MGI Ref ID J:94703)
  • cranioschisis
    • either completely open sagittal suture or incomplete closure at 7 weeks of age   (MGI Ref ID J:94703)
  • cardiovascular system phenotype
  • abnormal blood vessel morphology
    • delayed regression of vitreal vasculature, however the heart is histologically normal   (MGI Ref ID J:88367)
  • pigmentation phenotype
  • abnormal retinal pigment epithelium morphology
    • absence of the retinal pigment epithelium in a region encircling the optic nerve   (MGI Ref ID J:88367)
  • cellular phenotype
  • *normal* cellular phenotype
    • normal phosphatidyl serine flip-flop in thymocytes treated with dexamethasone   (MGI Ref ID J:59875)
    • E12.5 primary telencephalic cultures undergo normal cell death in response to AraC treatment   (MGI Ref ID J:66953)
    • decreased apoptosis
      • pyknotic clusters at sites of major morphogenetic change during brain development are not observed, indicating a decrease in apoptosis in the brain   (MGI Ref ID J:36821)
      • however, thymocytes show normal susceptibility to apoptosis   (MGI Ref ID J:36821)
  • hematopoietic system phenotype
  • abnormal osteoclast physiology
    • osteoclast activity is reduced, most likely due to dysfunctional preosteoblastic cells   (MGI Ref ID J:94703)
  • decreased thymocyte number
    • fewer total thymocytes at 2 weeks of age, however the spleen is histologically normal   (MGI Ref ID J:36821)
  • immune system phenotype
  • *normal* immune system phenotype
    • normal thymocyte expression patterns of CD4, CD8, CD25, CD69, and heat stable antigen   (MGI Ref ID J:36821)
    • abnormal osteoclast physiology
      • osteoclast activity is reduced, most likely due to dysfunctional preosteoblastic cells   (MGI Ref ID J:94703)
    • decreased thymocyte number
      • fewer total thymocytes at 2 weeks of age, however the spleen is histologically normal   (MGI Ref ID J:36821)
  • renal/urinary system phenotype
  • *normal* renal/urinary system phenotype
    • kidney is histologically normal   (MGI Ref ID J:36821)
  • respiratory system phenotype
  • *normal* respiratory system phenotype
    • lung is histologically normal   (MGI Ref ID J:36821)
  • reproductive system phenotype
  • *normal* reproductive system phenotype
    • testis is histologically normal   (MGI Ref ID J:36821)
View Research Applications

Research Applications
This mouse can be used to support research in many areas including:

Apoptosis Research
Endogenous Regulators

Cardiovascular Research
Ischemia studies

Developmental Biology Research
Eye Defects
Internal/Organ Defects
      ovary; uterus

Immunology, Inflammation and Autoimmunity Research
Intracellular Signaling Molecules

Reproductive Biology Research
Developmental Defects Affecting Gonads

Research Tools
Apoptosis Research
Reproductive Biology Research

Sensorineural Research
Cataracts
Eye Defects
Hearing Defects

Genes & Alleles

Gene & Allele Information provided by MGI

 
Allele Symbol Casp3tm1Flv
Allele Name targeted mutation 1, Richard Flavell
Allele Type Targeted (knock-out)
Common Name(s) CPP32-; Casp3-; caspase-3-;
Mutation Made ByDr. Richard Flavell,   Yale University School of Medicine
Strain of Origin129S1/Sv-Oca2<+> Tyr<+> Kitl<+>
ES Cell Line NameW9.5/W95
ES Cell Line Strain129S1/Sv-Oca2<+> Tyr<+> Kitl<+>
Gene Symbol and Name Casp3, caspase 3
Chromosome 8
Gene Common Name(s) A830040C14Rik; AC-3; Apopain; CC3; CPP32; CPP32B; Caspase-3; Lice; RIKEN cDNA A830040C14 gene; SCA-1; Yama; melody; mldy;
Molecular Note A genomic fragment containing sequences encoding a conserved motif was replaced with a neomycin selection cassette. RT-PCR analysis on samples derived from brain and liver of homozygous mice demonstrated that no detectable transcript is produced from this allele. Western blot analysis on samples derived from thymocytes of homozygous mice confirmed that no detectable protein was produced. [MGI Ref ID J:36821]

Genotyping

Genotyping Information

Genotyping Protocols

Casp3tm1Flv, Standard PCR


Helpful Links

Genotyping resources and troubleshooting

References

References provided by MGI

Selected Reference(s)

Kuida K; Zheng TS; Na S; Kuan C; Yang D; Karasuyama H; Rakic P; Flavell RA. 1996. Decreased apoptosis in the brain and premature lethality in CPP32-deficient mice. Nature 384(6607):368-72. [PubMed: 8934524]  [MGI Ref ID J:36821]

Additional References

Casp3tm1Flv related

Akhter A; Gavrilin MA; Frantz L; Washington S; Ditty C; Limoli D; Day C; Sarkar A; Newland C; Butchar J; Marsh CB; Wewers MD; Tridandapani S; Kanneganti TD; Amer AO. 2009. Caspase-7 activation by the Nlrc4/Ipaf inflammasome restricts Legionella pneumophila infection. PLoS Pathog 5(4):e1000361. [PubMed: 19343209]  [MGI Ref ID J:162695]

Amin S; Matalova E; Simpson C; Yoshida H; Tucker AS. 2007. Incudomalleal joint formation: the roles of apoptosis, migration and downregulation. BMC Dev Biol 7:134. [PubMed: 18053235]  [MGI Ref ID J:132300]

Carambula SF; Matikainen T; Lynch MP; Flavell RA; Goncalves PB; Tilly JL; Rueda BR. 2002. Caspase-3 is a pivotal mediator of apoptosis during regression of the ovarian corpus luteum. Endocrinology 143(4):1495-501. [PubMed: 11897708]  [MGI Ref ID J:109249]

Carambula SF; Pru JK; Lynch MP; Matikainen T; Goncalves PB; Flavell RA; Tilly JL; Rueda BR. 2003. Prostaglandin F2alpha- and FAS-activating antibody-induced regression of the corpus luteum involves caspase-8 and is defective in caspase-3 deficient mice. Reprod Biol Endocrinol 1:15. [PubMed: 12657159]  [MGI Ref ID J:102441]

D'Sa-Eipper C; Leonard JR; Putcha G; Zheng TS; Flavell RA; Rakic P; Kuida K; Roth KA. 2001. DNA damage-induced neural precursor cell apoptosis requires p53 and caspase 9 but neither Bax nor caspase 3. Development 128(1):137-46. [PubMed: 11092819]  [MGI Ref ID J:115386]

Delhase M; Kim SY; Lee H; Naiki-Ito A; Chen Y; Ahn ER; Murata K; Kim SJ; Lautsch N; Kobayashi KS; Shirai T; Karin M; Nakanishi M. 2011. TANK-binding kinase 1 (TBK1) controls cell survival through PAI-2/serpinB2 and transglutaminase 2. Proc Natl Acad Sci U S A :. [PubMed: 22203995]  [MGI Ref ID J:179973]

Fujita E; Egashira J; Urase K; Kuida K; Momoi T. 2001. Caspase-9 processing by caspase-3 via a feedback amplification loop in vivo. Cell Death Differ 8(4):335-44. [PubMed: 11550085]  [MGI Ref ID J:115634]

Guo YH; Hernandez I; Isermann B; Kang TB; Medved L; Sood R; Kerschen EJ; Holyst T; Mosesson MW; Weiler H. 2009. Caveolin-1-dependent apoptosis induced by fibrin degradation products. Blood 113(18):4431-9. [PubMed: 19074731]  [MGI Ref ID J:148438]

Jiao S; Li Z. 2011. Nonapoptotic function of BAD and BAX in long-term depression of synaptic transmission. Neuron 70(4):758-72. [PubMed: 21609830]  [MGI Ref ID J:174982]

Jo J; Whitcomb DJ; Olsen KM; Kerrigan TL; Lo SC; Bru-Mercier G; Dickinson B; Scullion S; Sheng M; Collingridge G; Cho K. 2011. Abeta(1-42) inhibition of LTP is mediated by a signaling pathway involving caspase-3, Akt1 and GSK-3beta. Nat Neurosci 14(5):545-7. [PubMed: 21441921]  [MGI Ref ID J:172292]

Kang SJ; Wang S; Kuida K; Yuan J. 2002. Distinct downstream pathways of caspase-11 in regulating apoptosis and cytokine maturation during septic shock response. Cell Death Differ 9(10):1115-25. [PubMed: 12232800]  [MGI Ref ID J:115554]

Khalil H; Peltzer N; Walicki J; Yang JY; Dubuis G; Gardiol N; Held W; Bigliardi P; Marsland B; Liaudet L; Widmann C. 2012. Caspase-3 Protects Stressed Organs against Cell Death. Mol Cell Biol 32(22):4523-33. [PubMed: 22949508]  [MGI Ref ID J:189241]

Kirkland RA; Saavedra GM; Cummings BS; Franklin JL. 2010. Bax regulates production of superoxide in both apoptotic and nonapoptotic neurons: role of caspases. J Neurosci 30(48):16114-27. [PubMed: 21123558]  [MGI Ref ID J:166748]

Koenig A; Fortner KA; King BR; Madden J; Buskiewicz IA; Budd RC. 2012. Proliferating gammadelta T cells manifest high and spatially confined caspase-3 activity. Immunology 135(4):276-86. [PubMed: 22117649]  [MGI Ref ID J:184101]

Koike M; Shibata M; Tadakoshi M; Gotoh K; Komatsu M; Waguri S; Kawahara N; Kuida K; Nagata S; Kominami E; Tanaka K; Uchiyama Y. 2008. Inhibition of autophagy prevents hippocampal pyramidal neuron death after hypoxic-ischemic injury. Am J Pathol 172(2):454-69. [PubMed: 18187572]  [MGI Ref ID J:131320]

Lakhani SA; Masud A; Kuida K; Porter GA Jr; Booth CJ; Mehal WZ; Inayat I; Flavell RA. 2006. Caspases 3 and 7: key mediators of mitochondrial events of apoptosis. Science 311(5762):847-51. [PubMed: 16469926]  [MGI Ref ID J:105496]

Lamkanfi M; Moreira LO; Makena P; Spierings DC; Boyd K; Murray PJ; Green DR; Kanneganti TD. 2009. Caspase-7 deficiency protects from endotoxin-induced lymphocyte apoptosis and improves survival. Blood 113(12):2742-5. [PubMed: 19168786]  [MGI Ref ID J:146876]

Le DA; Wu Y; Huang Z; Matsushita K; Plesnila N; Augustinack JC; Hyman BT; Yuan J; Kuida K; Flavell RA; Moskowitz MA. 2002. Caspase activation and neuroprotection in caspase-3- deficient mice after in vivo cerebral ischemia and in vitro oxygen glucose deprivation. Proc Natl Acad Sci U S A 99(23):15188-93. [PubMed: 12415117]  [MGI Ref ID J:126184]

Leonard JR; Klocke BJ; D'Sa C; Flavell RA; Roth KA. 2002. Strain-dependent neurodevelopmental abnormalities in caspase-3-deficient mice. J Neuropathol Exp Neurol 61(8):673-7. [PubMed: 12152782]  [MGI Ref ID J:104966]

Li F; He Z; Shen J; Huang Q; Li W; Liu X; He Y; Wolf F; Li CY. 2010. Apoptotic caspases regulate induction of iPSCs from human fibroblasts. Cell Stem Cell 7(4):508-20. [PubMed: 20887956]  [MGI Ref ID J:165654]

Li Z; Jo J; Jia JM; Lo SC; Whitcomb DJ; Jiao S; Cho K; Sheng M. 2010. Caspase-3 activation via mitochondria is required for long-term depression and AMPA receptor internalization. Cell 141(5):859-71. [PubMed: 20510932]  [MGI Ref ID J:167946]

Lin L; Ye Y; Zakeri Z. 2006. p53, Apaf-1, caspase-3, and -9 are dispensable for Cdk5 activation during cell death. Cell Death Differ 13(1):141-50. [PubMed: 16021178]  [MGI Ref ID J:121028]

Massa V; Savery D; Ybot-Gonzalez P; Ferraro E; Rongvaux A; Cecconi F; Flavell R; Greene ND; Copp AJ. 2009. Apoptosis is not required for mammalian neural tube closure. Proc Natl Acad Sci U S A 106(20):8233-8. [PubMed: 19420217]  [MGI Ref ID J:148528]

Matalova E; Sharpe PT; Lakhani SA; Roth KA; Flavell RA; Setkova J; Misek I; Tucker AS. 2006. Molar tooth development in caspase-3 deficient mice. Int J Dev Biol 50(5):491-7. [PubMed: 16586350]  [MGI Ref ID J:109513]

Matikainen T; Perez GI; Zheng TS; Kluzak TR; Rueda BR; Flavell RA; Tilly JL. 2001. Caspase-3 gene knockout defines cell lineage specificity for programmed cell death signaling in the ovary. Endocrinology 142(6):2468-80. [PubMed: 11356696]  [MGI Ref ID J:70205]

Miura M; Chen XD; Allen MR; Bi Y; Gronthos S; Seo BM; Lakhani S; Flavell RA; Feng XH; Robey PG; Young M; Shi S. 2004. A crucial role of caspase-3 in osteogenic differentiation of bone marrow stromal stem cells. J Clin Invest 114(12):1704-13. [PubMed: 15599395]  [MGI Ref ID J:94703]

Oppenheim RW; Flavell RA; Vinsant S; Prevette D; Kuan CY; Rakic P. 2001. Programmed cell death of developing mammalian neurons after genetic deletion of caspases. J Neurosci 21(13):4752-60. [PubMed: 11425902]  [MGI Ref ID J:70079]

Park E; Kim Y; Noh H; Lee H; Yoo S; Park S. 2013. EphA/ephrin-A signaling is critically involved in region-specific apoptosis during early brain development. Cell Death Differ 20(1):169-80. [PubMed: 22976838]  [MGI Ref ID J:205629]

Parker A; Hardisty-Hughes RE; Wisby L; Joyce S; Brown SD. 2010. Melody, an ENU mutation in Caspase 3, alters the catalytic cysteine residue and causes sensorineural hearing loss in mice. Mamm Genome 21(11-12):565-76. [PubMed: 21116635]  [MGI Ref ID J:166750]

Peterson SE; Yang AH; Bushman DM; Westra JW; Yung YC; Barral S; Mutoh T; Rehen SK; Chun J. 2012. Aneuploid cells are differentially susceptible to caspase-mediated death during embryonic cerebral cortical development. J Neurosci 32(46):16213-22. [PubMed: 23152605]  [MGI Ref ID J:192456]

Pompeiano M; Blaschke AJ; Flavell RA; Srinivasan A; Chun J. 2000. Decreased apoptosis in proliferative and postmitotic regions of the Caspase 3-deficient embryonic central nervous system. J Comp Neurol 423(1):1-12. [PubMed: 10861532]  [MGI Ref ID J:63081]

Roth KA; Kuan C; Haydar TF; D'Sa-Eipper C; Shindler KS; Zheng TS; Kuida K; Flavell RA; Rakic P. 2000. Epistatic and independent functions of caspase-3 and Bcl-X(L) in developmental programmed cell death. Proc Natl Acad Sci U S A 97(1):466-71. [PubMed: 10618441]  [MGI Ref ID J:59317]

Samuel MA; Morrey JD; Diamond MS. 2007. Caspase 3-dependent cell death of neurons contributes to the pathogenesis of West Nile virus encephalitis. J Virol 81(6):2614-23. [PubMed: 17192305]  [MGI Ref ID J:153324]

Simon DJ; Weimer RM; McLaughlin T; Kallop D; Stanger K; Yang J; O'Leary DD; Hannoush RN; Tessier-Lavigne M. 2012. A caspase cascade regulating developmental axon degeneration. J Neurosci 32(49):17540-53. [PubMed: 23223278]  [MGI Ref ID J:193196]

Srinivasan A; Roth KA; Sayers RO; Shindler KS; Wong AM; Fritz LC; Tomaselli KJ. 1998. In situ immunodetection of activated caspase-3 in apoptotic neurons in the developing nervous system. Cell Death Differ 5(12):1004-16. [PubMed: 9894607]  [MGI Ref ID J:82701]

Takahashi K; Kamiya K; Urase K; Suga M; Takizawa T; Mori H; Yoshikawa Y; Ichimura K; Kuida K; Momoi T. 2001. Caspase-3-deficiency induces hyperplasia of supporting cells and degeneration of sensory cells resulting in the hearing loss. Brain Res 894(2):359-67. [PubMed: 11251216]  [MGI Ref ID J:68122]

Tao Y; Zafar I; Kim J; Schrier RW; Edelstein CL. 2008. Caspase-3 gene deletion prolongs survival in polycystic kidney disease. J Am Soc Nephrol 19(4):749-55. [PubMed: 18272845]  [MGI Ref ID J:149924]

Unsain N; Higgins JM; Parker KN; Johnstone AD; Barker PA. 2013. XIAP regulates caspase activity in degenerating axons. Cell Rep 4(4):751-63. [PubMed: 23954782]  [MGI Ref ID J:202766]

Vince JE; Wong WW; Gentle I; Lawlor KE; Allam R; O'Reilly L; Mason K; Gross O; Ma S; Guarda G; Anderton H; Castillo R; Hacker G; Silke J; Tschopp J. 2012. Inhibitor of Apoptosis Proteins Limit RIP3 Kinase-Dependent Interleukin-1 Activation. Immunity 36(2):215-27. [PubMed: 22365665]  [MGI Ref ID J:181625]

Wickstrum JR; Bokhari SM; Fischer JL; Pinson DM; Yeh HW; Horvat RT; Parmely MJ. 2009. Francisella tularensis induces extensive caspase-3 activation and apoptotic cell death in the tissues of infected mice. Infect Immun 77(11):4827-36. [PubMed: 19703976]  [MGI Ref ID J:154196]

Wright KM; Vaughn AE; Deshmukh M. 2007. Apoptosome dependent caspase-3 activation pathway is non-redundant and necessary for apoptosis in sympathetic neurons. Cell Death Differ 14(3):625-33. [PubMed: 16932756]  [MGI Ref ID J:132340]

Yamaguchi Y; Shinotsuka N; Nonomura K; Takemoto K; Kuida K; Yosida H; Miura M. 2011. Live imaging of apoptosis in a novel transgenic mouse highlights its role in neural tube closure. J Cell Biol 195(6):1047-60. [PubMed: 22162136]  [MGI Ref ID J:178905]

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Zamboni DS; Kobayashi KS; Kohlsdorf T; Ogura Y; Long EM; Vance RE; Kuida K; Mariathasan S; Dixit VM; Flavell RA; Dietrich WF; Roy CR. 2006. The Birc1e cytosolic pattern-recognition receptor contributes to the detection and control of Legionella pneumophila infection. Nat Immunol 7(3):318-25. [PubMed: 16444259]  [MGI Ref ID J:112612]

Zandy AJ; Lakhani S; Zheng T; Flavell RA; Bassnett S. 2005. Role of the executioner caspases during lens development. J Biol Chem 280(34):30263-72. [PubMed: 15994297]  [MGI Ref ID J:101037]

Zeiss CJ; Neal J; Johnson EA. 2004. Caspase-3 in postnatal retinal development and degeneration. Invest Ophthalmol Vis Sci 45(3):964-70. [PubMed: 14985318]  [MGI Ref ID J:88367]

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Health & husbandry

Health & Colony Maintenance Information

Animal Health Reports

Room Number           FGB27

Colony Maintenance

Breeding & HusbandryWhen maintaining a live colony, heterozygous females are bred with either heterozygous or homozygous males. The donating investigator reports that homozygous females are poor mothers.
Mating SystemHeterozygote x Homozygote         (Female x Male)   30-AUG-10
Heterozygote x Heterozygote         (Female x Male)   15-MAY-09
Diet Information LabDiet® 5K52/5K67

Pricing and Purchasing

Pricing, Supply Level & Notes, Controls


Pricing for USA, Canada and Mexico shipping destinations View International Pricing

Live Mice

Price per mouse (US dollars $)GenderGenotypes Provided
Individual Mouse $232.00Female or MaleHeterozygous for Casp3tm1Flv  
$232.00Female or MaleHomozygous for Casp3tm1Flv  
Price per Pair (US dollars $)Pair Genotype
$464.00Heterozygous for Casp3tm1Flv x Heterozygous for Casp3tm1Flv  
$464.00Heterozygous for Casp3tm1Flv x Homozygous for Casp3tm1Flv  

Standard Supply

Repository-Live.
Repository-Live represents an exclusive set of over 1500 unique mouse models across a vast array of research areas. Breeding colonies provide mice for both large and small orders and fluctuate in size depending on current demand for each strain. If a Repository strain is not immediately available, then within 2 to 3 business days, you will receive an estimated availability timeframe for your inquiry or order along with various delivery options. Repository strains typically are delivered at 4 to 8 weeks of age and will not exceed 12 weeks of age on the day of shipping. We will note and try to accommodate requests for specific ages of Repository strains but cannot guarantee provision of these strains at specific ages. However, if cohorts of mice (5 or more of one gender) are needed at a specific age range for experiments, please let us know.

Pricing for International shipping destinations View USA Canada and Mexico Pricing

Live Mice

Price per mouse (US dollars $)GenderGenotypes Provided
Individual Mouse $301.60Female or MaleHeterozygous for Casp3tm1Flv  
$301.60Female or MaleHomozygous for Casp3tm1Flv  
Price per Pair (US dollars $)Pair Genotype
$603.20Heterozygous for Casp3tm1Flv x Heterozygous for Casp3tm1Flv  
$603.20Heterozygous for Casp3tm1Flv x Homozygous for Casp3tm1Flv  

Standard Supply

Repository-Live.
Repository-Live represents an exclusive set of over 1500 unique mouse models across a vast array of research areas. Breeding colonies provide mice for both large and small orders and fluctuate in size depending on current demand for each strain. If a Repository strain is not immediately available, then within 2 to 3 business days, you will receive an estimated availability timeframe for your inquiry or order along with various delivery options. Repository strains typically are delivered at 4 to 8 weeks of age and will not exceed 12 weeks of age on the day of shipping. We will note and try to accommodate requests for specific ages of Repository strains but cannot guarantee provision of these strains at specific ages. However, if cohorts of mice (5 or more of one gender) are needed at a specific age range for experiments, please let us know.

View USA Canada and Mexico Pricing View International Pricing

Standard Supply

Repository-Live.
Repository-Live represents an exclusive set of over 1500 unique mouse models across a vast array of research areas. Breeding colonies provide mice for both large and small orders and fluctuate in size depending on current demand for each strain. If a Repository strain is not immediately available, then within 2 to 3 business days, you will receive an estimated availability timeframe for your inquiry or order along with various delivery options. Repository strains typically are delivered at 4 to 8 weeks of age and will not exceed 12 weeks of age on the day of shipping. We will note and try to accommodate requests for specific ages of Repository strains but cannot guarantee provision of these strains at specific ages. However, if cohorts of mice (5 or more of one gender) are needed at a specific age range for experiments, please let us know.

Control Information

  Control
   005304 C57BL/6NJ
 
  Considerations for Choosing Controls
  Control Pricing Information for Genetically Engineered Mutant Strains.
 

Payment Terms and Conditions

Terms are granted by individual review and stated on the customer invoice(s) and account statement. These transactions are payable in U.S. currency within the granted terms. Payment for services, products, shipping containers, and shipping costs that are rendered are expected within the payment terms indicated on the invoice or stated by contract. Invoices and account balances in arrears of stated terms may result in The Jackson Laboratory pursuing collection activities including but not limited to outside agencies and court filings.


See Terms of Use tab for General Terms and Conditions


The Jackson Laboratory's Genotype Promise

The Jackson Laboratory has rigorous genetic quality control and mutant gene genotyping programs to ensure the genetic background of JAX® Mice strains as well as the genotypes of strains with identified molecular mutations. JAX® Mice strains are only made available to researchers after meeting our standards. However, the phenotype of each strain may not be fully characterized and/or captured in the strain data sheets. Therefore, we cannot guarantee a strain's phenotype will meet all expectations. To ensure that JAX® Mice will meet the needs of individual research projects or when requesting a strain that is new to your research, we suggest ordering and performing tests on a small number of mice to determine suitability for your particular project.
Ordering Information
JAX® Mice
Surgical and Preconditioning Services
JAX® Services
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Tel: 1-800-422-6423 or 1-207-288-5845
Fax: 1-207-288-6150
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Terms of Use

Terms of Use


General Terms and Conditions


For Licensing and Use Restrictions view the link(s) below:
- Use of MICE by companies or for-profit entities requires a license prior to shipping.

Contact information

General inquiries regarding Terms of Use

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phone:207-288-6470

JAX® Mice, Products & Services Conditions of Use

"MICE" means mouse strains, their progeny derived by inbreeding or crossbreeding, unmodified derivatives from mouse strains or their progeny supplied by The Jackson Laboratory ("JACKSON"). "PRODUCTS" means biological materials supplied by JACKSON, and their derivatives. "RECIPIENT" means each recipient of MICE, PRODUCTS, or services provided by JACKSON including each institution, its employees and other researchers under its control. MICE or PRODUCTS shall not be: (i) used for any purpose other than the internal research, (ii) sold or otherwise provided to any third party for any use, or (iii) provided to any agent or other third party to provide breeding or other services. Acceptance of MICE or PRODUCTS from JACKSON shall be deemed as agreement by RECIPIENT to these conditions, and departure from these conditions requires JACKSON's prior written authorization.

No Warranty

MICE, PRODUCTS AND SERVICES ARE PROVIDED “AS IS”. JACKSON EXTENDS NO WARRANTIES OF ANY KIND, EITHER EXPRESS, IMPLIED, OR STATUTORY, WITH RESPECT TO MICE, PRODUCTS OR SERVICES, INCLUDING ANY IMPLIED WARRANTY OF MERCHANTABILITY OR FITNESS FOR A PARTICULAR PURPOSE, OR ANY WARRANTY OF NON-INFRINGEMENT OF ANY PATENT, TRADEMARK, OR OTHER INTELLECTUAL PROPERTY RIGHTS.

In case of dissatisfaction for a valid reason and claimed in writing by a purchaser within ninety (90) days of receipt of mice, products or services, JACKSON will, at its option, provide credit or replacement for the mice or product received or the services provided.

No Liability

In no event shall JACKSON, its trustees, directors, officers, employees, and affiliates be liable for any causes of action or damages, including any direct, indirect, special, or consequential damages, arising out of the provision of MICE, PRODUCTS or services, including economic damage or injury to property and lost profits, and including any damage arising from acts or negligence on the part of JACKSON, its agents or employees. Unless prohibited by law, in purchasing or receiving MICE, PRODUCTS or services from JACKSON, purchaser or recipient, or any party claiming by or through them, expressly releases and discharges JACKSON from all such causes of action or damages, and further agrees to defend and indemnify JACKSON from any costs or damages arising out of any third party claims.

MICE and PRODUCTS are to be used in a safe manner and in accordance with all applicable governmental rules and regulations.

The foregoing represents the General Terms and Conditions applicable to JACKSON’s MICE, PRODUCTS or services. In addition, special terms and conditions of sale of certain MICE, PRODUCTS or services may be set forth separately in JACKSON web pages, catalogs, price lists, contracts, and/or other documents, and these special terms and conditions shall also govern the sale of these MICE, PRODUCTS and services by JACKSON, and by its licensees and distributors.

Acceptance of delivery of MICE, PRODUCTS or services shall be deemed agreement to these terms and conditions. No purchase order or other document transmitted by purchaser or recipient that may modify the terms and conditions hereof, shall be in any way binding on JACKSON, and instead the terms and conditions set forth herein, including any special terms and conditions set forth separately, shall govern the sale of MICE, PRODUCTS or services by JACKSON.


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